A study at the University of Iowa suggests that cells in the gut are actually protecting the brain from developing Parkinson’s disease (PD). Intestinal cells actually spark an immune response that protects the brain cells from damage that can cause PD. These intestinal cells investigate which parts of neurons are defective and discard the damaged parts.
The paper was published Aug. 30 in the journal Cell Reports. The title is ““The Mitochondria-Regulated Immune Pathway Activated in the C. elegans Intestine Is Neuroprotective.”
PD is a disease that erodes motor control and balance over time. As many as one million Americans live with the disease, according to the Parkinson’s Disease Foundation. More than ten million worldwide live with PD. About 60,000 Americans are diagnosed with PD every year, not counting the numerous cases that go undiagnosed.
The disease occurs when the neurons that control movement become impaired or die. Michael J. Fox is a notable person who has PD. Muhammad Ali also had PD, and some people wondered if boxing had something to do with it. The neurons normally produce dopamine, but when they are damaged or killed, the dopamine shortage leads to motor problems.
Damaged mitochondria, which are like the power centers of the cells, are linked to various nervous disorders, not just PD, and scientists want to understand why.
This study in roundworms dealt with a poison called rotenone, which researchers know kills neurons whose death is linked to PD. The poison damaged the mitochondria in the neurons. But, the damaged mitochondria did not damage all of the worm’s dopamine-producing neurons. On average, only seven percent lost dopamine-producing neurons when given rotenone.
An immune response was activated in the worms that discarded the damaged mitochondria, stopping a sequence that would’ve lost dopamine-producing neurons. The immune response originated not in the nervous system, but in the intestine.
The scientists are working on hypotheses as to why this happens. It could be the intestinal immune cells are constantly surveying the mitochondria for defects. This could be due to the bacterial origin of the mitochondria. It started as a bacterium and was only later integrated as a cell part. It’s possible that the intestinal cells don’t “trust” the mitochondria.
In TBI, the mitochondria may be damaged also promoting cell death. Targeted therapy using this research could prevent the cascade of events that lead to cell death and neurological dysfunction.
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